I. Field of the invention
This invention relates generally to the design of cardiac pacemakers, and more particularly to a dual-chamber atrioventricular (AV) sequential pacemaker having the capability of automatically adjusting the right heart AV interval in order to optimize the left heart AV interval. It accomplishes this by compensating for pacing-induced inter-atrial and inter-ventricular conduction delays known to produce impairment of ventricular function in prior art pacers.
II. Discussion of the Prior Art
The technique of cardiac pacing provides electrical stimulation of the myocardium when normal, intrinsic stimuli are absent or too slow. Beginning at the site of the stimulating electrode, an electrical wave, or depolarization, spreads through existing pathways in the myocardium as if the stimulus were natural. However, typical pacing electrodes are rarely placed near the site of origination of normal sinus beats. They are usually placed on the wall of the right atrial appendage or near the apex of the right ventricle. By virtue of this placement, an artificially stimulated depolarization must travel different distances across the heart, thus utilizing pathways that an intrinsic sinus beat would not.
A normal contraction cycle in the heart, shown in FIG. 1, begins at the sinoatrial node (302) in the wall of the right atrium (304) near the superior vena cava (306). Specialized nervous tissue located there has enhanced capacity to produce an action potential and thus is capable of overriding the ability of all cardiac muscle cells to initiate a contraction. Due to the enhanced ability of these cells to perform cyclical depolarization and repolarization, this locus is known as the heart's natural pacemaker. The depolarization spreads from this site at about 1 meter per second into both the right (308) and left (310) atria then atrial appendages (312, 314) causing atrial contraction. Thus, in normal subjects, right and left atrial contraction occurs within a period of 15 to 20 msec of each other.
The wave eventually reaches the atrioventricular (AV) junction (316), which is specialized for slow conduction. This is the only normal electrical connection between the atria and the ventricles and it assures that atrial contraction is completed before the ventricles are stimulated. As the stimulus is passed on to the ventricles, it reaches the specialized fibers of the bundle of His (318) and the Purkinje fibers (paths F-G-H and F-J-K). These fibers conduct at a much higher rate than the atrial muscle, about 5 meters per second. These specialized fibers form a network over the ventricles and thus distribute to clusters of true cardiac muscle (324, 332) the stimulus to depolarize. This process is not exactly simultaneous due to the fact that the stimulus tends to descend the right bundle branch (320-322) slightly more slowly (0.01 sec) than the left bundle branch (330-332). Therefore, the left and right surfaces of the interventricular septum (326) are stimulated differently so that the depolarization moves from left to right. However, this difference is not very apparent when considering the entire ventricular conduction period, because once the wave reaches the ventricular free walls (340, 350), it travels its perpendicular path more quickly on the right (350). This is due to the significantly smaller right muscle mass of the thinner right free wall and thus compensates somewhat for the prior delay. In this manner, normal ventricular depolarization is almost simultaneous and is completed in less than 0.1 second. Thus, the atrial to ventricular contraction sequence occurs almost simultaneously for left and right sides of the heart.
A typical lead configuration as known in the art for pacing both atrium and ventricle is shown in FIG. 2. A catheter 12 is fit into the right atrium and another catheter 14 in the tip of the right ventricle. Both may have one or two electrodes, one of them placed at each tip. Electrical stimuli may be delivered at either locus and Will be transferred by cardiac tissue in the normal manner, as described more fully hereinafter.
A summary of normal conduction pathways is provided by the heart shown in FIG. 3a. A normal depolarization is initiated at the sinoatrial node (A). It spreads to the right atrial appendage (B), the inter-atrial septum (C), the left atrium and appendage (D) and the atrioventricular node (E). It crosses into the ventricles and reaches the bundle of His (F). It then splits and runs parallel the two sides of the septum (F to G, G to H; F to J, J to K) following the right bundle branch (F to G to H) and the left bundle branch (F to J to K). It then spreads out to the Purkinje system and the individual cardiac muscle fibers of the right (I) and left (L) ventricles.
Cardiac pacing interferes with this normal cycle because typical paced beats are not initiated at the sinoatrial node (A) as native beats are. A typical atrial beat, therefore, is required to follow an abnormal depolarization pathway in order to reach the ventricles.
An example of such an abnormal depolarization pathway is that which results when a pacing electrode is placed on the right atrial appendage, as shown in FIG. 3b. The stimulus travels from the point of electrode placement A' towards the base of the appendage. As previously described, this conduction occurs by passing the stimulus from muscle cell to muscle cell at only about 1 meter per second in the healthy heart and possibly slower in the diseased heart. This results in a first depolarization and contraction cycle in the right atrium (A' to B', A' to C', A' to E) followed by a second depolarization and contraction cycle in the left atrium (C' to D, E to D). The delay between these two contractions (right and left atrium) has been found to be in the range of 70 to 200 msec.
Another example of an abnormal depolarization pathway is that which occurs during ventricular pacing, as shown in FIG. 3c. A similar delay as in atrial pacing has been observed when the right ventricle is paced. The apex of the right ventricle is stimulated (A") and the depolarization flows along the pathway G-H-I. It also flows retrograde through the bundle branches (A"to B") of the right Purkinje system up to the bundle of His (B") then to the left ventricular Purkinje system (B" to J to K). This results in a delay in depolarization and contraction between the two cavities of 60 to 100 msec. During this process, the much slower ability of cardiac muscle fibers to stimulate one another plays an insignificant role in passing the contraction stimulus through the interventricular septum and from right free wall to left free wall and from the point of stimulation to the left ventricle (A" to J).
This has important implications in treating pathological conditions, since every patient has an optimal AV delay. If the AV delay is either too short or too long, there will be a reduction of ventricular filling and thus a reduction in cardiac output, defined as the quantity of blood moved through the heart per unit of time. The atrial contribution to cardiac output (CO) is well known and has been one of the objectives of the development of dual-chamber, AV sequential pacemakers. However, it has become increasingly apparent that programming a pacemaker to be timed to preserve an AV interval that is within a "physiological" range may be misleading when based upon delivery of pacing pulses to the right atrium and/or ventricle, due to both the aforementioned delays in contraction and the known difficulty in assessing exact timing of left atrial and left ventricular depolarization from a standard surface ECG.
Furthermore, some pathological conditions are intermittent. A well-designed pacemaker should be able to detect then react as intermittent conduction problems spontaneously begin and end. An example of such a condition is intermittent heart block. One way to monitor these conditions is by the standard electrocardiogram depolarization waveform.
Cardiac pacemakers are designed to detect the movement of the depolarization as it spreads across the heart, utilizing the standard electrocardiography PQRST waveform. In certain pathological conditions such as heart block, there may be an excessive lengthening of AV interval causing various degrees of alteration in ventricular function, depending on the timing of the P waves in relation to the QRS complex. If there is an AV dissociation, those beats with properly timed P waves are known to be stronger than those without. Restoration of AV synchrony by artificial pacing in these patients usually improves cardiac function. It must be remembered, however, that true AV synchrony is only attained when the pacemaker used is programmed to account for the differences in conduction times inherent in the process of pacing.
When pacing the atrium and sensing the ventricle, it is possible to account for these differences by calculating the left heart AV interval (LAV) on the bases Of the measured total AV interval (AV) and inter-atrial conduction delay. Using the formula LAV=AV-IACT, it is possible to determine whether the stimulated beats are being conducted within an appropriate range.
Two examples are illustrative:
If the patient suffers from sinus bradycardia and the right atrium is paced with a lead in the right atrial appendage, the patient's own PR interval (i.e., typically 150 ms) will be apparently preserved, as seen on the surface ECG. Since the impulse is originated in the right atrial appendage, it takes some time to reach the left atrium (e.g. 100 ms), so the actual left heart AV interval (LAV) will be considerably shorter (50 ms) and outside the physiologic range.
Likewise, if the patient suffers from third degree AV block and AV sequential pacing is used, pacing the right ventricle 150 ms after a sensed P wave will lengthen left heart AV interval by the duration of inter-ventricular conduction time. Thus, actual left heart AV during atrial sensing-ventrical pacing is the result of adding the measured AV plus the interventricular conduction time.
It is apparent from above observations, that programming a pacemaker to preserve a "physiological" AV interval based on measurements of right-sided events may be misleading, since the left atrial and left ventricular depolarization are difficult to assess from a standard surface ECG. To more appropriately adjust the timing, it is important to know the factors that influence these intervals.
Research was done to separately measure right and left heart AV intervals during different pacing modalities and to assess left ventricular systolic function by systolic time intervals. Inter-atrial conduction time (IACT) was measured from the right atrial pacing spike to the onset of left atrial depolarization, as detected by an esophageal electrode.
Inter-ventricular conduction time is the additional delay caused by right ventricular pacing on the onset of left ventricular activation-contraction. This was assessed by measuring the duration of left heart pre-ejection period both during RV pacing and during spontaneous depolarization. The difference between these modes of initiating a contraction is thus an approximation of the inter-ventricular conduction time.
The above research has shown that in conditions of apparent physiological pacing as judged from right-sided AV intervals within a physiological range, non-physiological left heart AV intervals may result. Furthermore, it is well known that non-physiological left heart AV intervals may produce impairment of ventricular function. Thus, depending on whether the right atrium and right ventricle are paced or sensed, there will be alteration or not on the left heart AV interval. When the right atrium is sensed, there is no change in the left heart AV when the right ventricle is sensed as well, but the LAV will lengthen when the right ventricle is paced. When the right atrium is paced, there is a shortening in LAV when the right ventricle is sensed, but if the right ventricle is also paced, the delays may partially cancel out.